Activation of Satellite Cells in the Intercostal Muscles of Patients With Chronic Obstructive Pulmonary Disease

The respiratory muscles of patients with chronic obstructive pulmonary disease (COPD) display evidence of structural damage in parallel with signs of adaptation. We hypothesized that this can only be explained by the simultaneous activation of satellite cells. The aim of this study was to analyze th...

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Veröffentlicht in:Archivos de bronconeumología (English ed.) 2008-05, Vol.44 (5), p.239-244
Hauptverfasser: Martínez-Llorens, Juana, Casadevall, Carme, Lloreta, Josep, Orozco-Levi, Mauricio, Barreiro, Esther, Broquetas, Joan, Gea, Joaquim
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container_end_page 244
container_issue 5
container_start_page 239
container_title Archivos de bronconeumología (English ed.)
container_volume 44
creator Martínez-Llorens, Juana
Casadevall, Carme
Lloreta, Josep
Orozco-Levi, Mauricio
Barreiro, Esther
Broquetas, Joan
Gea, Joaquim
description The respiratory muscles of patients with chronic obstructive pulmonary disease (COPD) display evidence of structural damage in parallel with signs of adaptation. We hypothesized that this can only be explained by the simultaneous activation of satellite cells. The aim of this study was to analyze the number and activation of those cells along with the expression of markers of microstructural damage that are frequently associated with regeneration. The study included 8 patients with severe COPD (mean [SD] forced expiratory volume in 1 second, 33% [9%] of predicted) and 7 control subjects in whom biopsies were performed of the external intercostal muscle. The samples were analyzed by light microscopy to assess muscle fiber phenotype, electron microscopy to identify satellite cells, and real-time polymerase chain reaction to analyze the expression of the following markers: insulin-like growth factor 1, mechano growth factor, and embryonic and perinatal myosin heavy chains (MHC) as markers of microstructural damage; Pax-7 and m-cadherin as markers of the presence and activation of satellite cells, respectively; and MHC-I, IIa, and IIx as determinants of muscle fiber phenotype. The patients had larger fibers than healthy subjects (54 [6] vs 42 [4] μm 2; P < .01) with a similar or slightly increased proportion of satellite cells, as measured by ultrastructural analysis (4.3% [1%] vs 3.7% [3.5%]; P > .05) or expression of Pax-7 (5.5 [4.1] vs 1.6 [0.8] arbitrary units [AU]; P < .05). In addition, there was greater activation of satellite cells in the patients, as indicated by increased expression of m-cadherin (3.8 [2.1] vs 1.0 [1.2] AU; P=.05). This was associated with increased expression of markers of microstructural damage: insulin-like growth factor 1, 0.35 (0.34) vs 0.09 (0.08) AU ( P < .05); mechano growth factor, 0.45 (0.55) vs 0.13 (0.17) AU ( P=.05). CONCLUSIONS: The intercostal muscles of patients with severe COPD show indirect signs of microstructural damage accompanied by satellite cell activation. This suggests the presence of ongoing cycles of lesion and repair that could partially explain the maintenance of the structural properties of the muscle. Los músculos respiratorios de los pacientes con enfermedad pulmonar obstructiva crónica (EPOC) presentan lesiones estructurales, que coexisten con signos de adaptación. Nuestra hipótesis es que esto sólo puede explicarse si se produce simultáneamente la activación de sus células satélite. El propósito del
doi_str_mv 10.1016/S1579-2129(08)60038-5
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We hypothesized that this can only be explained by the simultaneous activation of satellite cells. The aim of this study was to analyze the number and activation of those cells along with the expression of markers of microstructural damage that are frequently associated with regeneration. The study included 8 patients with severe COPD (mean [SD] forced expiratory volume in 1 second, 33% [9%] of predicted) and 7 control subjects in whom biopsies were performed of the external intercostal muscle. The samples were analyzed by light microscopy to assess muscle fiber phenotype, electron microscopy to identify satellite cells, and real-time polymerase chain reaction to analyze the expression of the following markers: insulin-like growth factor 1, mechano growth factor, and embryonic and perinatal myosin heavy chains (MHC) as markers of microstructural damage; Pax-7 and m-cadherin as markers of the presence and activation of satellite cells, respectively; and MHC-I, IIa, and IIx as determinants of muscle fiber phenotype. The patients had larger fibers than healthy subjects (54 [6] vs 42 [4] μm 2; P < .01) with a similar or slightly increased proportion of satellite cells, as measured by ultrastructural analysis (4.3% [1%] vs 3.7% [3.5%]; P > .05) or expression of Pax-7 (5.5 [4.1] vs 1.6 [0.8] arbitrary units [AU]; P < .05). In addition, there was greater activation of satellite cells in the patients, as indicated by increased expression of m-cadherin (3.8 [2.1] vs 1.0 [1.2] AU; P=.05). This was associated with increased expression of markers of microstructural damage: insulin-like growth factor 1, 0.35 (0.34) vs 0.09 (0.08) AU ( P < .05); mechano growth factor, 0.45 (0.55) vs 0.13 (0.17) AU ( P=.05). CONCLUSIONS: The intercostal muscles of patients with severe COPD show indirect signs of microstructural damage accompanied by satellite cell activation. This suggests the presence of ongoing cycles of lesion and repair that could partially explain the maintenance of the structural properties of the muscle. Los músculos respiratorios de los pacientes con enfermedad pulmonar obstructiva crónica (EPOC) presentan lesiones estructurales, que coexisten con signos de adaptación. Nuestra hipótesis es que esto sólo puede explicarse si se produce simultáneamente la activación de sus células satélite. El propósito del presente trabajo ha sido valorar el número y la eventual activación de dichas células, así como la expresión de marcadores de microlesión estructural, ligados a la regeneración. Se incluyó en el estudio a 8 pacientes con EPOC grave -media ± desviación estándar del volumen espiratorio forzado en el primer segundo: un 33 ± 9% del valor de referencia-y a 7 controles, a quienes se realizó una biopsia del músculo intercostal externo. La muestra se analizó mediante microscopia óptica (fenotipo fibrilar), electrónica (células satélite) y técnica de reacción en cadena de la polimerasa en tiempo real (marcadores de microlesión: factor de crecimiento similar a la insulina de tipo 1, factor de crecimiento mecánico e isoformas de cadenas pesadas de miosina [MyHC] embrionaria e isoformas de perinatal; de presencia y activación de células satélite: Pax-7 y m-caderina, respectivamente; y condicionantes del fenotipo fibrilar: MyHC-I, IIa y IIx). Los pacientes tuvieron unas fibras mayores que los sujetos sanos (54 ± 6 frente a 42 ± 4 |a, m 2; p < 0,01), con una población de células satélite conservada o ligeramente incrementada (cuantificación ultraestructural: 4,3 ± 1% frente al 3,7 ± 3,5%, p no significativa; Pax-7: 5,5 ± 4,1 frente a 1,6 ± 0,8, unidades arbitrarias [ua], respectivamente, p < 0,05) y una mayor activación (m-caderina: 3,8 ± 2,1 frente a 1,0 ± 1,2 ua; p = 0,05). Esto se asociaba a valores aumentados de marcadores de microlesión (factor de crecimiento similar a la insulina de tipo 1: 0,35 ± 0,34 frente a 0,09 ± 0,08 ua, p < 0,05; factor de crecimiento mecánico: 0,45 ± 0,55 frente a 0,13 ± 0,17 ua, p = 0,05). Los músculos intercostales de pacientes con EPOC grave muestran signos indirectos de microlesión, acompañados de la activación de sus células satélite. Esto apunta a la presencia de ciclos continuados de lesión y reparación, lo que podría explicar parcialmente la conservación de sus propiedades estructurales.]]></description><identifier>ISSN: 1579-2129</identifier><identifier>ISSN: 0300-2896</identifier><identifier>EISSN: 1579-2129</identifier><identifier>DOI: 10.1016/S1579-2129(08)60038-5</identifier><identifier>PMID: 18448014</identifier><language>eng ; spa</language><publisher>Spain</publisher><subject>Aged ; Biopsy ; COPD ; Células satélite ; Damage ; Daño ; Disfunción muscular ; EPOC ; Female ; Humans ; Intercostal Muscles - drug effects ; Intercostal Muscles - metabolism ; Intercostal Muscles - pathology ; Intercostal Muscles - physiopathology ; Male ; Muscle dysfunction ; Muscle Fibers, Skeletal - pathology ; Phenotype ; Pulmonary Disease, Chronic Obstructive - drug therapy ; Pulmonary Disease, Chronic Obstructive - physiopathology ; Repair ; Reparación ; Satellite cells ; Satellite Cells, Skeletal Muscle - drug effects ; Satellite Cells, Skeletal Muscle - metabolism ; Satellite Cells, Skeletal Muscle - pathology</subject><ispartof>Archivos de bronconeumología (English ed.), 2008-05, Vol.44 (5), p.239-244</ispartof><rights>2008 Sociedad Española de Neumología y Cirugía Torácica (SEPAR)</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c293t-332e8d8a25a557797af0647429f14ec28347092355cd15f692a2ca448af7ffec3</citedby><cites>FETCH-LOGICAL-c293t-332e8d8a25a557797af0647429f14ec28347092355cd15f692a2ca448af7ffec3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S1579212908600385$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18448014$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Martínez-Llorens, Juana</creatorcontrib><creatorcontrib>Casadevall, Carme</creatorcontrib><creatorcontrib>Lloreta, Josep</creatorcontrib><creatorcontrib>Orozco-Levi, Mauricio</creatorcontrib><creatorcontrib>Barreiro, Esther</creatorcontrib><creatorcontrib>Broquetas, Joan</creatorcontrib><creatorcontrib>Gea, Joaquim</creatorcontrib><title>Activation of Satellite Cells in the Intercostal Muscles of Patients With Chronic Obstructive Pulmonary Disease</title><title>Archivos de bronconeumología (English ed.)</title><addtitle>Arch Bronconeumol</addtitle><description><![CDATA[The respiratory muscles of patients with chronic obstructive pulmonary disease (COPD) display evidence of structural damage in parallel with signs of adaptation. We hypothesized that this can only be explained by the simultaneous activation of satellite cells. The aim of this study was to analyze the number and activation of those cells along with the expression of markers of microstructural damage that are frequently associated with regeneration. The study included 8 patients with severe COPD (mean [SD] forced expiratory volume in 1 second, 33% [9%] of predicted) and 7 control subjects in whom biopsies were performed of the external intercostal muscle. The samples were analyzed by light microscopy to assess muscle fiber phenotype, electron microscopy to identify satellite cells, and real-time polymerase chain reaction to analyze the expression of the following markers: insulin-like growth factor 1, mechano growth factor, and embryonic and perinatal myosin heavy chains (MHC) as markers of microstructural damage; Pax-7 and m-cadherin as markers of the presence and activation of satellite cells, respectively; and MHC-I, IIa, and IIx as determinants of muscle fiber phenotype. The patients had larger fibers than healthy subjects (54 [6] vs 42 [4] μm 2; P < .01) with a similar or slightly increased proportion of satellite cells, as measured by ultrastructural analysis (4.3% [1%] vs 3.7% [3.5%]; P > .05) or expression of Pax-7 (5.5 [4.1] vs 1.6 [0.8] arbitrary units [AU]; P < .05). In addition, there was greater activation of satellite cells in the patients, as indicated by increased expression of m-cadherin (3.8 [2.1] vs 1.0 [1.2] AU; P=.05). This was associated with increased expression of markers of microstructural damage: insulin-like growth factor 1, 0.35 (0.34) vs 0.09 (0.08) AU ( P < .05); mechano growth factor, 0.45 (0.55) vs 0.13 (0.17) AU ( P=.05). CONCLUSIONS: The intercostal muscles of patients with severe COPD show indirect signs of microstructural damage accompanied by satellite cell activation. This suggests the presence of ongoing cycles of lesion and repair that could partially explain the maintenance of the structural properties of the muscle. Los músculos respiratorios de los pacientes con enfermedad pulmonar obstructiva crónica (EPOC) presentan lesiones estructurales, que coexisten con signos de adaptación. Nuestra hipótesis es que esto sólo puede explicarse si se produce simultáneamente la activación de sus células satélite. El propósito del presente trabajo ha sido valorar el número y la eventual activación de dichas células, así como la expresión de marcadores de microlesión estructural, ligados a la regeneración. Se incluyó en el estudio a 8 pacientes con EPOC grave -media ± desviación estándar del volumen espiratorio forzado en el primer segundo: un 33 ± 9% del valor de referencia-y a 7 controles, a quienes se realizó una biopsia del músculo intercostal externo. La muestra se analizó mediante microscopia óptica (fenotipo fibrilar), electrónica (células satélite) y técnica de reacción en cadena de la polimerasa en tiempo real (marcadores de microlesión: factor de crecimiento similar a la insulina de tipo 1, factor de crecimiento mecánico e isoformas de cadenas pesadas de miosina [MyHC] embrionaria e isoformas de perinatal; de presencia y activación de células satélite: Pax-7 y m-caderina, respectivamente; y condicionantes del fenotipo fibrilar: MyHC-I, IIa y IIx). Los pacientes tuvieron unas fibras mayores que los sujetos sanos (54 ± 6 frente a 42 ± 4 |a, m 2; p < 0,01), con una población de células satélite conservada o ligeramente incrementada (cuantificación ultraestructural: 4,3 ± 1% frente al 3,7 ± 3,5%, p no significativa; Pax-7: 5,5 ± 4,1 frente a 1,6 ± 0,8, unidades arbitrarias [ua], respectivamente, p < 0,05) y una mayor activación (m-caderina: 3,8 ± 2,1 frente a 1,0 ± 1,2 ua; p = 0,05). Esto se asociaba a valores aumentados de marcadores de microlesión (factor de crecimiento similar a la insulina de tipo 1: 0,35 ± 0,34 frente a 0,09 ± 0,08 ua, p < 0,05; factor de crecimiento mecánico: 0,45 ± 0,55 frente a 0,13 ± 0,17 ua, p = 0,05). Los músculos intercostales de pacientes con EPOC grave muestran signos indirectos de microlesión, acompañados de la activación de sus células satélite. Esto apunta a la presencia de ciclos continuados de lesión y reparación, lo que podría explicar parcialmente la conservación de sus propiedades estructurales.]]></description><subject>Aged</subject><subject>Biopsy</subject><subject>COPD</subject><subject>Células satélite</subject><subject>Damage</subject><subject>Daño</subject><subject>Disfunción muscular</subject><subject>EPOC</subject><subject>Female</subject><subject>Humans</subject><subject>Intercostal Muscles - drug effects</subject><subject>Intercostal Muscles - metabolism</subject><subject>Intercostal Muscles - pathology</subject><subject>Intercostal Muscles - physiopathology</subject><subject>Male</subject><subject>Muscle dysfunction</subject><subject>Muscle Fibers, Skeletal - pathology</subject><subject>Phenotype</subject><subject>Pulmonary Disease, Chronic Obstructive - drug therapy</subject><subject>Pulmonary Disease, Chronic Obstructive - physiopathology</subject><subject>Repair</subject><subject>Reparación</subject><subject>Satellite cells</subject><subject>Satellite Cells, Skeletal Muscle - drug effects</subject><subject>Satellite Cells, Skeletal Muscle - metabolism</subject><subject>Satellite Cells, Skeletal Muscle - pathology</subject><issn>1579-2129</issn><issn>0300-2896</issn><issn>1579-2129</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkE1P3DAQhi1EVb76E0A-IXpIsZ04sU_VaiktEmiRoOrRMs5Y6yobU4-D1H9f74coN04zGr3vzLwPIaecfeGMt5cPXHa6ElzoC6Y-t4zVqpJ75PB1vP-mPyBHiL8Za1vO-UdywFXTKMabQxJnLocXm0McafT0wWYYhpCBzktFGkaal0BvxgzJRcx2oHcTugFwrb4vPhgz0l8hL-l8meIYHF08YU7Tei3Q-2lYxdGmv_QqIFiEE_LB2wHh064ek5_X3x7nP6rbxfeb-ey2ckLXuaprAapXVkgrZdfpznrWNl0jtOcNOKHqpmNa1FK6nkvfamGFsyWU9Z334Opjcr7d-5zinwkwm1VAVzLZEeKEptVcKqV0Ecqt0KWImMCb5xRW5WPDmVmTNhvSZo3RMGU2pI0svrPdgelpBf1_1w5tEXzdCqDEfAmQDLpCy0EfErhs-hjeOfEPruOOjw</recordid><startdate>20080501</startdate><enddate>20080501</enddate><creator>Martínez-Llorens, Juana</creator><creator>Casadevall, Carme</creator><creator>Lloreta, Josep</creator><creator>Orozco-Levi, Mauricio</creator><creator>Barreiro, Esther</creator><creator>Broquetas, Joan</creator><creator>Gea, Joaquim</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>20080501</creationdate><title>Activation of Satellite Cells in the Intercostal Muscles of Patients With Chronic Obstructive Pulmonary Disease</title><author>Martínez-Llorens, Juana ; Casadevall, Carme ; Lloreta, Josep ; Orozco-Levi, Mauricio ; Barreiro, Esther ; Broquetas, Joan ; Gea, Joaquim</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c293t-332e8d8a25a557797af0647429f14ec28347092355cd15f692a2ca448af7ffec3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng ; spa</language><creationdate>2008</creationdate><topic>Aged</topic><topic>Biopsy</topic><topic>COPD</topic><topic>Células satélite</topic><topic>Damage</topic><topic>Daño</topic><topic>Disfunción muscular</topic><topic>EPOC</topic><topic>Female</topic><topic>Humans</topic><topic>Intercostal Muscles - drug effects</topic><topic>Intercostal Muscles - metabolism</topic><topic>Intercostal Muscles - pathology</topic><topic>Intercostal Muscles - physiopathology</topic><topic>Male</topic><topic>Muscle dysfunction</topic><topic>Muscle Fibers, Skeletal - pathology</topic><topic>Phenotype</topic><topic>Pulmonary Disease, Chronic Obstructive - drug therapy</topic><topic>Pulmonary Disease, Chronic Obstructive - physiopathology</topic><topic>Repair</topic><topic>Reparación</topic><topic>Satellite cells</topic><topic>Satellite Cells, Skeletal Muscle - drug effects</topic><topic>Satellite Cells, Skeletal Muscle - metabolism</topic><topic>Satellite Cells, Skeletal Muscle - pathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Martínez-Llorens, Juana</creatorcontrib><creatorcontrib>Casadevall, Carme</creatorcontrib><creatorcontrib>Lloreta, Josep</creatorcontrib><creatorcontrib>Orozco-Levi, Mauricio</creatorcontrib><creatorcontrib>Barreiro, Esther</creatorcontrib><creatorcontrib>Broquetas, Joan</creatorcontrib><creatorcontrib>Gea, Joaquim</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Archivos de bronconeumología (English ed.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Martínez-Llorens, Juana</au><au>Casadevall, Carme</au><au>Lloreta, Josep</au><au>Orozco-Levi, Mauricio</au><au>Barreiro, Esther</au><au>Broquetas, Joan</au><au>Gea, Joaquim</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Activation of Satellite Cells in the Intercostal Muscles of Patients With Chronic Obstructive Pulmonary Disease</atitle><jtitle>Archivos de bronconeumología (English ed.)</jtitle><addtitle>Arch Bronconeumol</addtitle><date>2008-05-01</date><risdate>2008</risdate><volume>44</volume><issue>5</issue><spage>239</spage><epage>244</epage><pages>239-244</pages><issn>1579-2129</issn><issn>0300-2896</issn><eissn>1579-2129</eissn><abstract><![CDATA[The respiratory muscles of patients with chronic obstructive pulmonary disease (COPD) display evidence of structural damage in parallel with signs of adaptation. We hypothesized that this can only be explained by the simultaneous activation of satellite cells. The aim of this study was to analyze the number and activation of those cells along with the expression of markers of microstructural damage that are frequently associated with regeneration. The study included 8 patients with severe COPD (mean [SD] forced expiratory volume in 1 second, 33% [9%] of predicted) and 7 control subjects in whom biopsies were performed of the external intercostal muscle. The samples were analyzed by light microscopy to assess muscle fiber phenotype, electron microscopy to identify satellite cells, and real-time polymerase chain reaction to analyze the expression of the following markers: insulin-like growth factor 1, mechano growth factor, and embryonic and perinatal myosin heavy chains (MHC) as markers of microstructural damage; Pax-7 and m-cadherin as markers of the presence and activation of satellite cells, respectively; and MHC-I, IIa, and IIx as determinants of muscle fiber phenotype. The patients had larger fibers than healthy subjects (54 [6] vs 42 [4] μm 2; P < .01) with a similar or slightly increased proportion of satellite cells, as measured by ultrastructural analysis (4.3% [1%] vs 3.7% [3.5%]; P > .05) or expression of Pax-7 (5.5 [4.1] vs 1.6 [0.8] arbitrary units [AU]; P < .05). In addition, there was greater activation of satellite cells in the patients, as indicated by increased expression of m-cadherin (3.8 [2.1] vs 1.0 [1.2] AU; P=.05). This was associated with increased expression of markers of microstructural damage: insulin-like growth factor 1, 0.35 (0.34) vs 0.09 (0.08) AU ( P < .05); mechano growth factor, 0.45 (0.55) vs 0.13 (0.17) AU ( P=.05). CONCLUSIONS: The intercostal muscles of patients with severe COPD show indirect signs of microstructural damage accompanied by satellite cell activation. This suggests the presence of ongoing cycles of lesion and repair that could partially explain the maintenance of the structural properties of the muscle. Los músculos respiratorios de los pacientes con enfermedad pulmonar obstructiva crónica (EPOC) presentan lesiones estructurales, que coexisten con signos de adaptación. Nuestra hipótesis es que esto sólo puede explicarse si se produce simultáneamente la activación de sus células satélite. El propósito del presente trabajo ha sido valorar el número y la eventual activación de dichas células, así como la expresión de marcadores de microlesión estructural, ligados a la regeneración. Se incluyó en el estudio a 8 pacientes con EPOC grave -media ± desviación estándar del volumen espiratorio forzado en el primer segundo: un 33 ± 9% del valor de referencia-y a 7 controles, a quienes se realizó una biopsia del músculo intercostal externo. La muestra se analizó mediante microscopia óptica (fenotipo fibrilar), electrónica (células satélite) y técnica de reacción en cadena de la polimerasa en tiempo real (marcadores de microlesión: factor de crecimiento similar a la insulina de tipo 1, factor de crecimiento mecánico e isoformas de cadenas pesadas de miosina [MyHC] embrionaria e isoformas de perinatal; de presencia y activación de células satélite: Pax-7 y m-caderina, respectivamente; y condicionantes del fenotipo fibrilar: MyHC-I, IIa y IIx). Los pacientes tuvieron unas fibras mayores que los sujetos sanos (54 ± 6 frente a 42 ± 4 |a, m 2; p < 0,01), con una población de células satélite conservada o ligeramente incrementada (cuantificación ultraestructural: 4,3 ± 1% frente al 3,7 ± 3,5%, p no significativa; Pax-7: 5,5 ± 4,1 frente a 1,6 ± 0,8, unidades arbitrarias [ua], respectivamente, p < 0,05) y una mayor activación (m-caderina: 3,8 ± 2,1 frente a 1,0 ± 1,2 ua; p = 0,05). Esto se asociaba a valores aumentados de marcadores de microlesión (factor de crecimiento similar a la insulina de tipo 1: 0,35 ± 0,34 frente a 0,09 ± 0,08 ua, p < 0,05; factor de crecimiento mecánico: 0,45 ± 0,55 frente a 0,13 ± 0,17 ua, p = 0,05). Los músculos intercostales de pacientes con EPOC grave muestran signos indirectos de microlesión, acompañados de la activación de sus células satélite. Esto apunta a la presencia de ciclos continuados de lesión y reparación, lo que podría explicar parcialmente la conservación de sus propiedades estructurales.]]></abstract><cop>Spain</cop><pmid>18448014</pmid><doi>10.1016/S1579-2129(08)60038-5</doi><tpages>6</tpages></addata></record>
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identifier ISSN: 1579-2129
ispartof Archivos de bronconeumología (English ed.), 2008-05, Vol.44 (5), p.239-244
issn 1579-2129
0300-2896
1579-2129
language eng ; spa
recordid cdi_proquest_miscellaneous_69158889
source MEDLINE; Elsevier ScienceDirect Journals
subjects Aged
Biopsy
COPD
Células satélite
Damage
Daño
Disfunción muscular
EPOC
Female
Humans
Intercostal Muscles - drug effects
Intercostal Muscles - metabolism
Intercostal Muscles - pathology
Intercostal Muscles - physiopathology
Male
Muscle dysfunction
Muscle Fibers, Skeletal - pathology
Phenotype
Pulmonary Disease, Chronic Obstructive - drug therapy
Pulmonary Disease, Chronic Obstructive - physiopathology
Repair
Reparación
Satellite cells
Satellite Cells, Skeletal Muscle - drug effects
Satellite Cells, Skeletal Muscle - metabolism
Satellite Cells, Skeletal Muscle - pathology
title Activation of Satellite Cells in the Intercostal Muscles of Patients With Chronic Obstructive Pulmonary Disease
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